| 1. |
- Rutqvist, LE
(författare)
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Adjuvant endocrine therapy
- 2004
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Ingår i: Best practice & research. Clinical endocrinology & metabolism. - 1521-690X. ; 18:1, s. 81-95
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Tidskriftsartikel (refereegranskat)
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| 2. |
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| 3. |
- Ahrén, Bo
(författare)
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Clinical results of treating type 2 diabetic patients with sitagliptin, vildagliptin or saxagliptin - diabetes control and potential adverse events
- 2009
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Ingår i: Best Practice and Research in Clinical Endocrinology and Metabolism. - : Elsevier BV. - 1521-690X. ; 23:4, s. 487-498
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Tidskriftsartikel (refereegranskat)abstract
- Inhibition of dipeptidyl peptidase-4 (DPP-4) is a novel oral treatment for type 2 diabetes. DPP-4 inhibition increases insulin secretion and reduces glucagon secretion by preventing the inactivation of glucagon-like peptide-1 (GLP-1), thereby lowering glucose levels. Several DPP-4 inhibitors are in clinical development; more studies exist for sitagliptin and vildagliptin. They improve metabolic control in type 2 diabetes in monotherapy and also in combination with metformin, sulphonylurea and thiazolidinediones. HbA(1c) is reduced by approximately 0.6-1.1% in studies up to 52 weeks. Similar, although more limited, results were obtained for saxagliptin. DPP-4 inhibitors are safe and tolerable with no increased risk of adverse events compared to placebo and have a low risk of hypoglycaemia. DPP-4 inhibitors are body weight-neutral. The DPP-4 inhibitors are recommended for use in the early stage of type 2 diabetes, in combination with metformin in subjects with inadequate glycaemic control. DPP-4 inhibition may also be used in combination with sulphonylurea and thiazolidinediones and potentially also in combination with insulin. The durability and long-term safety of DPP-4 inhibitors remain to be established.
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| 4. |
- Ahrén, Bo
(författare)
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DPP-4 inhibitors.
- 2007
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Ingår i: Baillière's Best Practice & Research in Clinical Endocrinology & Metabolism. - : Elsevier BV. - 1521-690X. ; 21:4, s. 517-533
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Tidskriftsartikel (refereegranskat)abstract
- Inhibition of dipeptidyl peptidase 4 (DPP-4) is a novel treatment for type-2 diabetes. DPP-4 inhibition prevents the inactivation of glucagon-like peptide 1 (GLP-1), which increases levels of active GLP-1. This increases insulin secretion and reduces glucagon secretion, thereby lowering glucose levels. Several DPP-4 inhibitors are in clinical development. Most experience so far has been with sitagliptin (Merck; approved by the FDA) and vildagliptin (Novartis; filed). These are orally active compounds with a long duration, allowing once-daily administration. Both sitagliptin and vildagliptin improve metabolic control in type-2 diabetes, both in monotherapy and in combination with metformin and thiazolidinediones. A reduction in HbA(1c) of approximately 1% is seen in studies of DPP-4 inhibition of up to 52 weeks' duration. DPP-4 inhibition is safe and well tolerated, the risk of hypoglycaemia is minimal, and DPP-4 inhibition is body-weight neutral. DPP-4 inhibition is suggested to be a first-line treatment of type-2 diabetes, particularly in its early stages in combination with metformin. However, the durability and long-term safety of DPP-4 inhibition remain to be established.
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| 5. |
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| 6. |
- Beardsall, Kathryn, et al.
(författare)
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Insulin and carbohydrate metabolism
- 2008
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Ingår i: Baillière's Best Practice & Research. Clinical Endocrinology & Metabolism. - : Elsevier BV. - 1521-690X .- 1532-1908. ; 22:1, s. 41-55
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Forskningsöversikt (refereegranskat)abstract
- Fetal glucose exposure and consequent fetal insulin secretion is normally tightly regulated by glucose delivery from the mother during pregnancy. Maternal hyperglycaemia and gestational diabetes (GDM) are known to be detrimental to offspring, although defining the criteria for diagnosis of GDM is controversial. Recent data suggest that the risk of poor fetal outcome appears to be a continuous variable across the range of glucose control, and that the level of maternal blood glucose for a diagnosis of gestational diabetes needs to be reviewed. After birth, rapid adaptation is necessary for infants to be able to maintain independent glucose homeostasis. This adaptation is compromised in infants who are small for gestational age (SGA), premature, or large for gestational age (LGA). Interestingly, the infants who are born at the extremes of birth weight are also at increased risk of impaired glucose tolerance and diabetes in later life.
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| 7. |
- Borgstrom, F, et al.
(författare)
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Health economics of osteoporosis
- 2008
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Ingår i: Best practice & research. Clinical endocrinology & metabolism. - : Elsevier BV. - 1878-1594 .- 1521-690X. ; 22:5, s. 885-900
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Tidskriftsartikel (refereegranskat)
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| 8. |
- Brommage, Robert, et al.
(författare)
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Translational studies provide insights for the etiology and treatment of cortical bone osteoporosis
- 2018
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Ingår i: Best Practice & Research Clinical Endocrinology & Metabolism. - : Elsevier BV. - 1521-690X. ; 32:3, s. 329-340
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Tidskriftsartikel (refereegranskat)abstract
- Increasing attention is being focused on the important contributions of cortical bone to bone strength, fractures and osteoporosis therapies. Recent progress in human genome wide association studies in combination with high-throughput mouse gene knockout phenotyping efforts of multiple genes and advanced conditional gene inactivation in mouse models have successfully identified genes with crucial roles in cortical bone homeostasis. Particular attention in this review is given to genes, such as WNT16, POSTN and SFRP4, that differentially affect cortical and trabecular bone architecture. We propose that animal models of cortical bone metabolism will substantially contribute to developing anabolic osteoporosis therapies that improve cortical bone mass and reduce non-vertebral fracture risk. 0 (C) 2018 Elsevier Ltd. All rights reserved.
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| 9. |
- Bunderen, Christa C. van, et al.
(författare)
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Meta-analysis of mortality in adults with growth hormone deficiency: Does growth hormone replacement therapy really improve mortality rates?
- 2023
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Ingår i: BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM. - 1521-690X .- 1532-1908. ; 37:6
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Tidskriftsartikel (refereegranskat)abstract
- Growth hormone (GH) deficiency (GHD) is one of the most prevalent deficiencies in patients with hypopituitarism and several cohort studies have demonstrated an increased mortality risk in hypopituitary pa-tients with a presumed GHD. The cause of the excess mortality is most likely multifactorial, including the etiology of the hypopituitarism, non-physiological replacement therapies (mostly glucocorticoid), tumor treatment and its side effects as well as untreated GHD. Several years later, other cohort studies that investigated life expectancy in patients with hypopituitarism on GH replacement therapy (GHRT) that showed a normalized mortality. By comparison of the distribution of char-acteristics of interest between cohorts, we discuss the existing literature to answer the following question: does growth hormone replacement really improve mortality rates in adult patients with hypopituitarism and GHD? We also conducted a meta-analysis of these studies. Since the literature suffers from selection and time bias (improvement of tumor management and other pituitary hormone replacement therapies), there is no high-quality evidence that replacement therapy for GHD really improves mortality. However, the available data does suggest that GHRT plays a significant part in the normalization of the mortality in patients with hypopituitarism.
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| 10. |
- Ekblom, BT
(författare)
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Blood boosting and sport
- 2000
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Ingår i: Bailliere's best practice & research. Clinical endocrinology & metabolism. - : Elsevier BV. - 1532-1908 .- 1521-690X. ; 14:1, s. 89-98
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Tidskriftsartikel (refereegranskat)
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